Tuesday, 24 November 2015


Public Health England published the latest figures for 

Common animal-associated infections quarterly reports: 2015

Lyme borreliosis (Borrelia burgdorferi) Total cases of positive serology in the first 3 quarters of 2015 = 606

 of these 429 were considered to be Acute infections.
Lyme disease (data from the Rare and Imported Pathogens Laboratory, Porton) 
'During the third quarter of 2015, a total of 421 cases of laboratory confirmed Lyme disease were reported, compared with 300 during the third quarter of 2014. Of these cases, 340 were acute (including 30 neuroborreliosis) and 81 were past infections. Of the acute cases, 182 were male (aged 2- 90 years, median 46) and 151 were female (aged 1- 93 years, median 51). Gender was unrecorded for seven cases and age was unrecorded for one case.' 

'Thirty-four (10%) of the acute cases reported foreign travel. The majority of cases had travelled in Europe (n=24), eight had travelled in the Americas, one had been to the Middle East, and one to the Far East. One hundred and fifty-six acute cases reported an insect bite, of whom 145 specified a tick bite. Sixty-eight cases reported erythema migrans as a presenting symptom.'

These figures leave far more questions than answers. -

PHE refer to cases that were not considered to be acute cases as past infection - that is quite misleading because there is no test used by NHS that can say the infection was a past infection. The normal rules of antibody responses do not always apply with Lyme disease - the immune system shows an undulatory immune response in early disease and has not been researched in late disease, although cases are documented of further IgM spikes in later disease as is found in Relapsing fever Borreliosis.

340 acute cases of which 68 reported erythema migrans ie 20% suggest that maybe rather less than the 60% often quoted of people develop a erythema rash
 - but as Lyme Disease Action say in recent tweets
'NB this only lab reports. Aim to reduce this to zero - those with EM should be treated without blood test.'
 '% of acute cases sent for a blood test when they have EM ideally = zero. EM Should be treated w'out test.'
'See lymediseaseaction.org.uk/wp-content/upl under "What needs to be done No, 1" Hope it explains.'

Why are doctors sending blood to be tested when patients have presented with an EM rash? - NHS guidance says to treat, testing is not required and is unlikely to be positive in the first few weeks when treatment is necessary to try to prevent further sequale.

Anecdatol reports suggest that many doctors are not prepared to consider treatment unless they have a positive test result and others have been reported to withdraw treatment even with an EM rash because the test result comes back negative, completely contrary to the NHS guidance.

Estimates of actual Lyme Disease cases are considered by CDC and a previous head of Lyme reference unit in Scotland to be 10x that of serological positive cases

How blind our governments are to the Economic costs of this disease - http://lookingatlyme.blogspot.co.uk/2015/02/economic-costs-of-lyme-disease-lessons.html 

I posted about the figures in 2011 with information on figures in other European countries to compare how low reported cases in UK are by comparison -why?

also earlier figures http://lookingatlyme.blogspot.co.uk/2012/03/lyme-disease-increases-again-in-uk.html

and http://lookingatlyme.blogspot.co.uk/2011/12/concern-over-increasing-lyme-disease-in.html 

Monday, 16 November 2015


                   Photo courtesy of Mark Christian

Lifting The Veil II  

at the Academy Of Nutritional Medicine on Sunday 15th November 

Just a brief summary of this excellent conference - the presentations will shortly be available on the AONM website http://www.aonm.org  and a DVD will eventually be available from that website.

Professor B.K. Puri

Discussed ECG 
History - 1887 Augustus Waller first discovered the use of ECG at St Marys London carrying out the first ECG on a dog and then moved to humans. He also mapped the electrical field around the heart and produced a heart graph using PQRST.

Long QT Syndrome is found in 1 in 2500 of the population and can be hereditary.
Can cause rapid heart beat, seizures, respiratory arrest.

All SSRI's ( Selective serotonin reuptake inhibitors) can cause LQT interval.
All anti psychotic medication can cause LQT interval
Erythromycin orally can cause LQT interval a 300% higher risk of death from this than in patients taking Amoxycillin.
Environmental exposure to certain metals eg lead can increase risk of LQT interval.

Discussed Atrioventricular block
He discussed a paper in 1990 written by Dr Allen Steere on a case of AV block leading to death after an appendectomy - which said that Lyme Carditis must be considered especially in young patients with AV block.

Discussed a further cardiac study didn't catch the authors name 20% had right induction delay but after 2 weeks treatment ECG returned to normal.

Dr Monro

Discussed at length food intolerances, allergies and sensitivities under various headings Rationale, Investigations and treatment.

Harboring toxins may need detox procedures
Can't ignore the fact a person who has Lyme had intolerances before infection.
Can have homeostasis working when healthy but can be dragged down by infection.
Need to lift whole thing up simultaneously to lift patient up.
Food sensitivities - historically we all know about this - various intolerances 
Celiac has been associated with schizophrenia and a study found they improved when they couldn't get wheat during the war.
Studies have been done on wheat free and milk free.
In Celiac and in autism cases wheat free diet gave some improvements. 

The Breakspear clinic hold a massive collection of books and papers ( not all found on Pub med)
She recommended a book Not all in the Mind by Richard Mackarness

Anaphylactic shock was first described in 1901 and is an affect of the Autonomic nervous system. It was recognised in 1940 as a histamine release.
Discussed oral tolerances, no mast cells under the tongue so can use that to introduce oral tolerances.
Low dose immunotherapy.
Started with hay fever introduced weaker dilutions and can be used as a vaccine.
discussed two pathways ANS and Lymphocytes.
Emphasized people with chronic infections have allergies and these must be addressed.
Quoted 1/3 of the population had migraine. 1/3 of the population had IBS

Dr Klinghardt 


Started by giving a tribute to the work of Dr Jean Monro 
He did his thesis on the Autonomic nervous system (ANS) and the immune system, his colleagues thought ANS outdated - it was the beginning of a career in ANS. In Germany growing up he became interested in homeopathy, acupuncture and ANS.
Moving to the US different legal systems only allowed to use his hands so adopted his methodology.

Talks about 3 components
1. Genetic and epigenetic
2. Environmental challenge
3. The immune response to toxins, microbes, parasites.

"The response of the host makes the disease" Lewis Thomas MD -NEJM 1972.

Treating chronic Illnesss he uses 4 principles
1. Basic physiology - exercise, diet, trauma, work and transgenerational physiologies, hormones, vitamins, osteopathy,EMR protection
2. Decreasing toxic body burden- metals,chemicals & Biotoxins from extra and intra cellular matrix, EMR protection.
3. Immune Modulation- up regulating blocked or underactive immune function & down regulating hyperactive ones 
4. Decreasing microbial burden  diagnosisn & treating parasites, mould, viruses,( HSV, EBV etc) bacteria eg Borrelia, bartonella, protozone ( Babesia, toxoplasmosa, omeba)

Stressed the importance of paleo diet and benefits of Japaneese knotweed for long term treatment to keep Lyme at bay. also a need for using antivirals.

1. Toxicity
2. Unresolved psycho evolutionary & trans generation issues
3. EMR microwave, electricity & magnetic fields
4. Infections
6. HPU (HemoPyrrollactanUria)
8. Dental issues
9. ? Brain waves
10.Decreased regulatory neuropeptides & hormonal deficiencies

Says he believes it is a mistake to try to fix hormonal issues ie in Babesia - hormones can make more toxic and need to come later in treatment.

Illness & Epigenetics

psychological and physical trauma

In animal models epimutations followed 7 generations generally led to study families dying out.
We are now third generation exposed to microwave and glyphosate 
Epimutations 1000x more significant than genetic mutations.
We do not have epigenetic testing yet.

Need to look at ways to help methylation.

Chlorella and chelation for heavy metals.
Aluminium particularly related with neuro toxins & pro inflammatory but no testing.

Tests that can help are 
Elevated MCV
elevated fasting blood sugar 90-110
low alkaline phosphate
moderately elevated LDC
Low urine specific gravity

are often indicated in the sickest patients.

Artimisin helpful and mentions a Lyme cocktail found on his website (link above)

John Caudwell

Spoke briefly about the journey he and his family had been on for the last 6 weeks. He has quickly recognised the lack of help from NHS and acknowledged how caring the lyme community was, he expects to interview for Chief Executive next week for a new charity for Lyme whose aim will be to get NHS to take responsibility for this patient group. He has been moved by the numbers of tragic stories. Much of what he said can be read on his Facebook page.

Dr Sarah Myhill

Sometimes I am ashamed to be a doctor - the biggest problem is the medical profession. Driven by pharmaceutical drugs to treat symptoms- it is important to ask what is the mechanisms going wrong.

Fatigue we all have, energy demand outstrips energy delivery 
Chronic fatigue - many have immunological symptoms.
ME also have inflammatory symptoms.

1. Very poor stamina
2. delayed fatigue
are only two symptoms looked for.

Energy loss
Muscles - No stamina, weakness
brain - Foggy brain, poor energy delivered to brain. Having low mood or depression may be way of conserving energy such as in low seasonal defective disorder.
eye - inability to read watch TV, photophobia- light intolerances
ear- noise intolerances
Immune system - activate immune system, such as in flu you
Intolerance heat & cold - requires energy. 
Gut & Liver- eating toxic food puts greater demands on liver
Hormone synthesis - likely to be slow
Cardiac symptoms - extremely common Heart symptoms compound all other symptoms. POTS - autonomic problem but can be a symptom of lack of energy to the heart.

Symptoms of inflammation can be localised or generalised. She draws a great analogy to a car engine  in respect of Mitachondria, diet, gut, lungs,heart circulation,Thyroid,Adrenal.

Need to pace energy but also mental energy. But refers to PACE as an oxymoron because if you get better with PACE therapy you do not have CFS.

Discusses various books she has written highlights importance of diet.
Modern diseases fueled by carbohydrate & sugar diets. Most important to follow stone age diet.
sleep - imperative 
Circadian rhythm
Sunshine & light vit D anti inflammatory, 
Avoid infections- acute infection is one thing but can switch on a chronic immune reaction.
(In generally ie flu or a cold she believes that symptoms of acute infection should not be suppressed by drugs, need to go to bed and rest, need to let immune system work).

Discussed tools to treat poor energy levels included CoQ10,Vit B3, magnesium, D ribose, vit B12 She says even if you can't get testing done this selection is very helpful and unlikely to do any harm.

Major source of toxins from fermenting gut. Alcohol intolerance is recognsied in ME patients uniformly.
Discussed thyroid function indicating problems with testing and the need to go on clinical symptoms. TSH is set high in UK and everyone has their own individual range.
Adrenal function - stress - mitochondria output
Detoxify- saunas can get rid of toxic load but not heavy metals.

Dr Schwartzbach 

Dr Schwardtzbach has tested more than 1000 samples from the UK and astounded how many tests are positive.

He gave an overview of infections and viruses that it is important to consider testing for in chronic diseases such as ME, MS, Fibromyalgia, RA,Alzheimers, Parkinsons, Autism.
Quoted that 50% of people in Sweden have Lyme Disease.  
It is a big problem to diagnose parasites only one lab that does that which is Fry labs in US.
Says CD57+ NK cells very important.
Learn from TB that it is reaction on T cells not B cells.
Only study on CD57 was one done by Stricker.
CD57 can be low in Chlamydia & Mycoplasma - need studies.

Elispot is test for T cells
very established, actual activity of T cells fighting against actual infections
sensitivity -84%
specificity -94%
Most doctors say it is unspecific everybody has it - but there is no argument to say this.
Patients not positive but have low CD57 if they are treated they improve and CD57 raises.
It uses the same bands that are used in the Western Blot.
antigen from B31 strain, OspA, Sensu stricto, Afzelii,garinii, + OspC native + DbpA? recombinant

The tests are CE certified - he does not produce the test he just uses them.

Tests support a clinical diagnosis
Doctors need to learn to make a clinical diagnosis it is not easy and no time to asses it needs specialists.

Immunoblot time will end in a year of two not because there is no Lyme.
Denmark don't use the Western blot they only use the ELISA based on only one study which was done by the person who owns the lab that does the tests.

Spot Technique
can quantify 60% in Chronic with 99% specificity

20%-30% Lyme positive in Autism - Bransfield
90% CFS Lyme positive
2014 - Pure Lyme dementia exists& has good outcomes in treated patients. Dementia patients should be tested.

Seems Koala bears can be treated for Chlamydia but not so humans.

Common symptoms of Chlamydia are cough, sinusitis and can cause all symptoms and illness as Lyme Borreliosis
Garth Nicolson - Mycoplasma
Can keep ticks in polythene bag in freezer/fridge? for testing

Bartonella was found in 40% of ticks in Germany.
Showed a slide of Bartonella striae which are common.
Babesia very Important for blood transfusions services.
EBV not found in ticks yet
Cytomegalovirus (CMV)
Herpes Simplex Virus linked with MS co factor CFS, Fibromyalgia
Coxsackie Virus nearly everyone in UK has IgA for CV

Most Fibromyalgia patients are Lyme positive.

Lyme found in Otzi died 50 million years ago.
oldest tick with Lyme found from 40 million years ago

Important to look for co infections too.
Autism 50% have chlamydia as well as 10-20% Borrelia but need to look for other infections

To treat viruses - barbour, artemisin, samento very difficult to eliminate - blocking mitochondria.

Dr Newton

Gave a brief update of a result of a visit to Porton Down in June. There will be a new initiative to try and raise funds for work on a UK direct testing method to find Borrelia this will be launched in a few days 


Dr Alan MacDonald

presentation by Vimeo with question and answers by skype.

Review of Infectious Borrelia species Chronic Brain Infections and the Development of Alzheimer's Disease from Alan MacDonald on Vimeo.

Saturday, 7 November 2015


'Lyme borreliosis should be considered in symptomatic  patients that have 

had exposure to ticks and not just those with a definite tick bite.'

Distribution and presentation of Lyme borreliosis in Scotland - analysis of data from a national testing laboratory.

Mavin S, Watson EJ, Evans R.


This study examines the distribution of laboratory-confirmed cases of Lyme borreliosis in Scotland and the clinical spectrum of presentations within NHS Highland. Methods General demographic data (age/sex/referring Health Board) from all cases of Lyme borreliosis serologically confirmed by the National Lyme Borreliosis Testing Laboratory from 1 January 2008 to 31 December 2013 were analysed. Clinical features of confirmed cases were ascertained from questionnaires sent to referring clinicians within NHS Highland during the study period. Results The number of laboratory-confirmed cases of Lyme borreliosis in Scotland peaked at 440 in 2010. From 2008 to 2013 the estimated average annual incidence was 6.8 per 100,000 (44.1 per 100,000 in NHS Highland). Of 594 questionnaires from NHS Highland patients: 76% had clinically confirmed Lyme borreliosis; 48% erythema migrans; 17% rash, 25% joint, 15% neurological and 1% cardiac symptoms. Only 61% could recall a tick bite. Conclusion The incidence of Lyme borreliosis may be stabilising in Scotland but NHS Highland remains an area of high incidence. Lyme borreliosis should be considered in symptomatic patients that have had exposure to ticks and not just those with a definite tick bite.

Thank you Scotland another insightful piece of research in this very important field.

Not everyone recalls a tick bite and not everyone gets an Erythema Migrans rash.

Currently there is much debate over the inadequacy of the current testing,  a two tired system of testing antibodies called the ELISA and the Western Blot.

This is an interesting paper 

Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection


Lyme Disease caused by infection with Borrelia burgdorferi is an emerging infectious disease and already by far the most common vector-borne disease in the U.S. Similar to many other infections, infection with Bburgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure. However, clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies. This is further supported by reports of frequent repeat infections with B.burgdorferi in endemic areas. The mechanisms underlying such a lack of long-term humoral immunity, however, remain unknown. We show here that Bburgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates. These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain ofBburgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of Bburgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction. Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that Bburgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.

Although this study is more concerned about long lived Immunity it also highlights other problems with B cell or antibody responses - '“This study also suggests a possible mechanism responsible for the disappearance of antibodies following infection and subsequent treatment with antibiotics,” 

'For months after infection, those germinal centers fail to produce the specific cells—memory B cells and antibody-producing plasma cells—that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria and launching a protective immune response against future infections with the pathogen'
There have been comments made that as patients become more ill their antibody response weakens and the Embers monkey study found that in monkeys infected but left untreated their antibody response weakened or leveled off. Link to the study - http://lookingatlyme.blogspot.co.uk/2012/01/proof-of-persistence-chronic-lyme.html

Over twenty years ago antibody response to Borrelia were already recognised as being problematic. 
Second European Symposium on Lyme Borreliosis A NATO advanced research workshop held on 19 and 20 May 1993 at St George's Hospital Medical School, University of London, United Kingdom (Organising committee John S Axford and David H E Rees (co-chairmen), Allen C Steere, Klaus Hansen, Susan Henderson (administrator))
page 398
Even though Lyme disease has been clearly identified as an infectious disease, there are still many riddles to be solved, especially with regard to the immune response to this organism. These include the question why only a small proportion of subjects originally exposed to B burgdorfenr progress to later disease stages, the genetic background, and the apparent dissociation between the cellular and humoral immune reactivity and a tremendous, but nevertheless restricted and apparently non-protective, antibody repertoire.
 Thus patients with Lyme borreliosis showed a significantly raised T cell response to whole B burgdorferi bacteria as compared with patients with other inflammatorv joint diseases and with normal controls. 
This dissociation of the humoral and the cellular immune response may be explained by several mechanisms. Initial experiments using T cell clones in patients with chronic Lyme disease suggest a selective activation of a certain T cell subset that produces a restricted pattern of cytokines which are unable to activate B cells.6 This selective expansion of responding cells may depend on the HLA profile as suggested by the high association of chronic Lyme arthritis refractory to antibiotic treatment with certain HLA-DR2 and DR4 alleles.7 In addition to an unusual T and B cell response, there is a peculiar uptake mechanism of B burgdorferi by phagocytes, which may explain some of the subsequent specific immune reactions.

page 399
It is an interesting finding that in the late stages of spirochaetal diseases, such as syphilis and, notably, Lyme disease, few infectious organisms are detectable in the lesional sites. There is often a strong local immune response, however, with a sometimes vigorous synovial inflammatory hypertrophy in Lyme arthritis which is histologically indistinguishable from rheumatoid synovitis.9 Apparently, just a few bacteria are sufficient to attract vast numbers of cells to the areas affected. It may be either a general immunosuppressive state that does not allow for a complete elimination of the microbe-or, alternatively, the immune system is directed into the wrong direction and uses false or inadequate means for elimination. Thus the study of Lyme disease, especially its arthritic manifestations, has provided important lessons about an inadequacy of the immune response towards elimination of microbial organisms in a chronic infection. These observations may provide important insights into other arthritides which are triggered by contact with infectious agents.

 There were some very interesting presentations made at this Symposium held in London  but very little has followed in respect of translating this into meaningful help to protect the British public from the devasation of this disease.

Tuesday, 27 October 2015


Published on Oct 14, 2015
Dr. Mozayeni talks about Bartonella as one of the major co-infections of Lyme disease. It's more prevalent than Lyme, as there are many more ways to contract the disease (eg. flees, cats). In a study, that Dr. Breitschwerdt and himself published in The Journal of Emerging Diseases, about 60% of Lyme patients tested positive for Bartonella.
Dr. Mozayeni also talks about the importance of looking at Biofilm when treating Lyme, Bartonella etc as biofilm can harbor many of these microbes and be the cause of many symptoms.

Dr Mozayeni -

Bartonella spp. bacteremia and rheumatic symptoms in patients from Lyme disease-endemic region.

Transcript from above video presentation:-

Dr Robert Mozayeni was treating patients with Lyme Disease in a Lyme endemic area  and developed a partnership with veterinarian Prof Ed Breitschewerdt.

A partnership of One Health with MD's working with Veterinarians.

Dr Mozayeni started sending blood samples to Prof Ed Breitschwerdt to be tested for Bartonella, over 20% were positive - more than any other in any patient group, including high risk veterinarians.

Dr Mozayeni subsequently published a paper (see above link.) up to 62% of patients had significant proof of laboratory testing for Bartonella - some had failed Lyme testing  - some had psychiatric symptoms.

I see Bartonella more prevalent than Lyme and while Lyme is a big problem, Borrelia meaning  Lyme = Borreliosis. I think that the Bartonella is a much bigger Public Health problem over all, because there are more ways to get Bartonella than even Borrelia, including other insects- fleas and cats.

There are germs in the environment, the insects carry the germs just like all other animals, farm animals and rodents. The more you are exposed to these things the more likely you pick up these infections and so it's great to be in nature, but you being in nature also means being with the microbes and so the risks are there and they are poly microbial. So we have to start thinking about these single germs. We need to think each germ we know about is representative of a broader group of germs and we need to start looking at a Microbiome - look at all the germ genes. So as of this year you may get whole gene sequencing for about $1000 and it used to be millions of dollars 10 years ago.
( Short discussion on possible further developments)

We realise when we talk about Lyme disease it is a much bigger set of microbes and the public refers to all of that as Lyme Disease, but that confuses definitions and creates controversy, because the medical definitions are very narrow, the public definition is a social networking definition - so even patients when told they have Bartonella will still call it, when they tell their friends they have Lyme Disease.

Now for example Norvect is named after Vectors. ILADS is Lyme & Associated Diseases. So these groups started very narrow with Borrelia so now they are broadening their view and I think that in general the medical community is seeing this too. For example we know now that it is scientifically established that Atherosclerosis is due to chronic infections in the vascular system. Some of it will turn out to be Bartonella some of it will turn out to be other germs. Some of it is from Bio films that have been produced from protozoa and then the Bio film gets contaminated by microbes and the body can't clear it because the biofilms are a physical barrier to the immune system. So we are now realising and appreciating the role of biofilms. If you search Pub med 25000 on biofilms since 1975. But if you search Biofilm and Lyme there have been 8 publications in just the last couple of years. So there is a massive awareness of biofilm problems but clinically no one really looks at it.

We have started a biofilm lab in January 2014 and we have now measured 400, 500 specimens and I can tell you the biofilms are a big problem and they are directly responsible for many symptoms and they harbor microbes. So all of the talks we have about all of these specific germs are still incomplete because you have Biofilms in the picture of biofilms an example of biofilms is the layer that thrombus - lines the blood vessel which then causes inflammation which can lead to atherosclerosis. So even Atherosclerosis has now been recognised as a chronic infection.

In many chronic illness we are realising they have an underlying infectious cause, you know maybe MS maybe RA so there are are areas where people have always wondered but now we are going back with better tools and searching again. 

People have misunderstood  and confused symptoms with diagnosis so when you call something Fibromyalgia it's just a set of symptoms it is not a diagnosis. If you call something Chronic Fatigue it's only a set of symptoms it is not a diagnosis. In fact there are few things in medicine  where the name of the disease  is actually a diagnosis and by that I mean a diagnosis, as actually identifying a root cause. So no matter what you call it you have to realise that everything we do with medicine is a classification system. To try to understand things we classify it and we may classify, but all the classifications may have to be considered temporary until we find  a root cause.

So when you are a sick patient and you get a label of say Fibromyalgia you have to ask yourself what causes Fibromyalgia and there's research that looks at describing Fibromyalgia better, and there's research that may seek to test and find  an underlying cause of Fibromyalgia. So when you get to a root cause you have a chance of being able to reverse. 

So most physicians will label it and do whatever the guidelines say for that set of symptoms which is a classification not a diagnosis of a root cause and then they've done what they feel was medically prudent and they've satisfied the lawyers and the policy makers and they can go home and sleep that night. But some of us we can't do that unless we fix the problem we don't sleep well at night, we have a patient who is ill and we haven't found the cause. And some of us we try to do that we have to look hard and this is where you end up doing things that are not in the guidelines, because you are exploring new possibilities and if you are trained as a medical scientist you are just naturally curious and once you have learned that medically they can't take it out of you. This is where sometimes the regulatory agencies and the policy makers have problems with practitioners because they are trying to limit what they do to try to regulate, control and reduce costs. So they are practicing statistics on individual patients, that is what they want done, but if you are an individual physician trying to solve a problem for a patient you have to take a personalised approach and you can't apply epidemiology and statistics to the patients - to every patient.

The policy makers have to think in broad terms but practitioners are trying to treat individual patients. So there is this constant tension between the broad approach versus solving an individual case at a time and we were trained to trust our own evaluation more than anything else - more than lab data - but the auditors and the policy makers just want to audit you with lab data, because that's the easiest thing for them to do.

So in a way the doctors in the front line are responsible for taking care of the patient. But the policy makers are forgetting that they are responsible for doing the research that help those doctors take care of the patients. So in my opinion they may be, some of them are forgetting their  real mission. But they do it because they think they are doing the right thing, are trying to protect the public and keep the cost down and limit the use of anything that is not fully validated. But for it to be fully validated a paper could take 17-21 years and if you are a sick patient their paradox is it's too bad you didn't live at the right time.

Friday, 23 October 2015


Tick abundances in South London parks and the potential risk for Lyme borreliosis to the general public 
  • C. NELSON, 
  • S. BANKS, 
  • T. WALKER and
  • J. G. LOGAN 
  • Abstract

    Tick abundances and prevalences of infection with Borrelia burgdorferi sensu lato, the causative agent of Lyme disease, were investigated in four South London parks. A total of 360 transects were sampled using three methods of collection (blanket, leggings and flags) simultaneously. No ticks were found on Wimbledon Common or at Hampton Court, but 1118 Ixodes ricinus (Ixodida: Ixodidae) ticks were collected at Richmond and Bushy Parks. At Richmond Park, lower canopy humidity [odds ratio (OR) 0.94; P = 0.005], increased mat depth (OR 1.15; P < 0.001) and increased soil moisture (OR 1.40; P = 0.001) predicted the presence of I. ricinus, and increased sward height [incidence rate ratio (IRR) 1.01; P = 0.006] and decreased ground temperature (IRR 0.90; P = 0.009) predicted increased abundance. At Bushy Park, thicker mat depth predicted tick presence (OR 1.17; P = 0.006) and increasing temperature correlated with tick absence (OR 0.57; P = 0.023). A total of 279 ticks were screened for the presence of B. burgdorferi using quantitative polymerase chain reaction. Point prevalences of 0% for larvae (n = 78), 2.14% for nymphs (n = 174) and 0% for adult ticks (n = 7) related to an acarological risk of 0.22 infected ticks per 40 m transect in Richmond Park. The abundance of ticks and the acarological risk, particularly at Richmond Park, highlight the need for appropriate communication of the associated risk to the general public frequenting these recreational areas.
    Interesting research on ticks in London Parks by researchers from the London school of Hygiene & Tropical medicine.
    James Logan has discussed his research in the media recently to help raise awareness of ticks and possible tick borne infections - Lyme Disease.
     Science daily - 'Dr James Logan, Senior Lecturer in Medical Entomology at the London School of Hygiene & Tropical Medicine, senior author of the study said: "The overall risk of Lyme disease in London parks is very low, but precautions should be taken. Check yourself and your pets after frequenting parkland areas, and remove any ticks as quickly as possible using a tick removal tool. To minimise the risk stick to footpaths and wear an insect repellent."
    Hopefully more such important work will be done and more awareness raised of Lyme Disease.
    In 1994 

    Evidence for Lyme disease in urban park workers: a potential new health hazard for city inhabitants.Rees DH1Axford JS.


    In the UK, cases of Lyme disease have only been reported from rural areas. Recently, however, Ixodes ticks infected with Borrelia burgdorferi have been found in London parks. To determine whether this constituted a health hazard, we questioned 44 workers from Richmond and Bushey parks to assess their exposure to tick bites and whether they had a clinical history of Lyme disease. Their serum was subsequently investigated for antibodies to two different preparations of Borrelia burgdorferi (whole cell sonicate and flagellin) and the specificity of these antibodies determined by immunoblotting. Comparison was made to zoo keepers (n = 27) from a wildlife park outside London. Tick bites were reported in 23% of park workers and of these, three described symptoms compatible with Lyme disease. Raised antibody levels were found in 10 (24%) of the park workers compared with one (4%) of the zoo keepers using ELISA with whole cell sonicate as antigen (P = 0.02) and 6 (14%) of park workers and none of the zoo keepers using purified flagellin as antigen (P < 0.05). Analysis of the immunoblots revealed more bands were detected in park workers (mean 1.8, range 0-6) than in the zoo keeper controls (mean 0.8, range 0-4); P < 0.001 and 14 (32%) of the park workers had reactivity with three or more protein bands, whilst only one of the zoo keepers showed this level of antigen binding (P < 0.005). These data suggest previous infection with B. burgdorferi in London park workers which has important health implications for these individuals, other park workers and possibly park visitors.

    20 years later and still no signage in the London parks.

    Anecdotal comments from patients infected in the London Parks show that there is still little doctor awareness too in that area. 

    Concerns that knowledge of tick borne disease in the UK will frighten people away from visiting the great outdoors seems to have been the policy of HPA but this is assumption and research does not support that concern. 

    So for 20 years the public are left ignorant and doctors are ill informed and ill equipped to help diagnose and treat Lyme Disease. 

    The human health burden rises year on year rarely seeming to magically resolve without treatment leaving a miserable existence for those infected and left untreated and a burden on our Health care costs benefit costs and economy. 

    Yesterday a meeting at the House of Lords on Lyme Disease asked the Health minister to respond to concerns - lack of awareness, public signage in the London Parks and lack of doctor awareness were just some of the many concerns.